Chf_treatment_2005

Treatment of Congestive Heart Failure
When you provide treatment for any medical or dental problem, it is useful to apply an organized approach. A common approach is: conservative, pharmacological and invasive treatment. This lecture will try to use this approach for the treatment of both acute and chronic heart failure. This handout is divided first into acute CHF and second, chronic CHF. Questions or comments to: jwaech@yahoo.ca. Objectives:
• identify the pathophysiological problems that exist in heart failure • understand how each form of treatment addresses the pathophysiology of CHF • understand how acute and chronic heart failure treatments are different
Acute CHF
Clinical scenario: a 70 year old female patient is brought into the emergency room because of severe breathing problems. In your history, you discover that she has had 2 large MI’s in the past and has an ejection fraction of 35% as a result of these MI’s. She takes the following medications: ACE inhibitor, beta blocker, ASA, and a diuretic. On physical exam she appears extremely distressed and is diaphoretic. Her vitals are: HR 100, BP 150/90, RR 30, SpO2 85%. She has coarse crackles throughout both lungs and an
S3. Her JVP is up to her ear in the sitting position and her ankles are swollen. Her liver is swollen and tender. Your impression is that this patient has severe acute congestive heart failure and is essentially drowning. Not all patients with acute heart failure have all the same problems, but there are many common factors which can be addressed:
• a triggering event that precipitated the acute episode (e.g. MI or infection) • decreased cardiac output • increased ventricular wall stress caused by
o increased preload o increased afterload (usually, but not always)
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General Principles:
• the heart is not functioning as a good pump. Cardiac output is abnormally low and
the filling pressures (preload) for the ventricles are abnormally high. As a result, fluid backs up under pressure and collects in the lungs. This causes pulmonary edema, dyspnea, hypoxia and distress. The primary goals will be to: reduce pulmonary edema, reduce preload, improve cardiac output, and relieve the patient’s symptoms.

Conservative treatments:
• body position: a patient who lies flat will have increased venous return to the
thorax. This will increase preload. Therefore, sitting up with the legs hanging over the side of the bed will help redistribute blood volume away from the thorax and reduce preload. It is better to have edema of the ankles than edema of the lungs for these patients. Use gravity to your advantage.
• rest: a lower metabolic rate will require a lower cardiac output. • oxygen: although possibly considered a drug, I will classify oxygen therapy as
conservative. Oxygen is given to improve all organ tissue oxygen levels, but specifically myocardial oxygenation. Oxygen is required for actin-myosin dissociation and thus cardiac relaxation. An ischemic myocardium will not fully relax during diastole and therefore, higher filling pressures will be required to fill the ventricle due to diastolic dysfunction. Therefore, oxygen therapy can help to decrease filling pressures in an ischemic heart. Further, an ischemic heart will have decreased contractility, so oxygen therapy may help to increase contractility and CO in an ischemic heart.
Pharmacological Treatments:
• please review the CVS pharmacology handout for details on drugs • diuretic: Will result in increased urine production and decreased blood volume,
leading to decreased preload. In addition to this mechanism, many diuretics also has a vasodilatory property which promotes preload and afterload reduction.
• nitroglycerine (NTG): is primarily a venodilator (venodilator means veins only, as
opposed to vasodilator which could mean veins and/or arterioles). Remember that veins are considered “capacitance” vessels. This means they can hold a volume of blood when they are dilated. A patient who is sympathetically stimulated due to stress will have venoconstriction due to α1 agonism and this will result in blood being redistributed centrally, to the thorax. Patients in acute CHF will have sympathetic stimulation and thus and venoconstriction. Dilation of these veins will redistribute the blood away from the thorax and reduce preload. Decreasing preload will also decrease ventricular wall stress. NTG can be given as a spray under the tongue, as a pill under the tongue, as a skin patch (slow onset) or as an intravenous infusion.
• morphine: is a narcotic which also has the unique property of resulting in
histamine release. Acting on the brain, morphine results in euphoria, decreased dyspnea and decreased respiratory drive via mu (µ) receptors. A decreased respiratory rate results in less oxygen consumed for the work of breathing. Also,
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because morphine is euphoric it decreases psychological stress and therefore sympathetic nervous stimulation. Decreased sympathetic stimulation results in less venous and arterial constriction, decreasing both preload and afterload and ventricular wall stress and will also lower heart rates. Histamine is a vasodilator which further reduces preload and afterload.
• nesiritide: is a B-type natriuretic analog. Is a new drug. Results in vasodilation
and diuresis. It is short acting and administered via an intravenous infusion. Not listed in the pharmacology handout and will not be on the exam. Still in clinical trials.
• • inotropes: dopamine and dobutamine are the most commonly used. Both result in
increased contractility and therefore cardiac output. Both are administered intravenously through a “central line” (large IV into a central vein such as internal jugular, subclavian or femoral) as an infusion and have very short half lives. Dopamine will increase cardiac output and blood pressure. Because dobutamine is also a vasodilator, it does not increase blood pressure, but will decrease preload and afterload and increase cardiac output. One “simplified” way to think of these 2 drugs is that dobutamine = dopamine + NTG.
 Note #1: all drugs that reduce preload will reduce ventricular diastolic volume
and pressure. Because coronary flow occurs during diastole, and the perfusion gradient for the coronary arteries is aortic diastolic pressure minus ventriculardiastolic pressure, reducing preload will also increase coronary blood flow by increasing the pressure gradient.
 Note #2: decreasing the afterload will result in improved ventricular ejection, a
larger stroke volume and an increased cardiac output.
 Note #3: all drugs that decrease preload or afterload have the potential to cause hypotension. A patient in acute decompensated heart failure may have low blood pressure and this will limit the use of drugs which lower preload and afterload.

Invasive Treatments:
• Invasive monitoring: preload (which is most accurately defined as end-diastolic
volume (EDV)) can be estimated by filling pressure. We can measure this non-invasively using the JVP to estimate preload of the right ventricle and we often assume that preload of the right ventricle mirrors the preload for the left ventricle. We can place a catheter in the internal jugular vein down the superior vena cava into the right atrium and directly measure filling pressures of the RV. However, to obtain a more direct measurement of LV preload, we use a pulmonary artery catheter (a.k.a. Swan-Ganz catheter) which is inserted in the internal jugular vein, and feeds through the RA, RV and finally into the pulmonary artery. From this position, the catheter can measure something called “pulmonary artery wedge pressure” which estimates LV preload. A value greater than 12 is abnormal. The pulmonary artery catheter can also measure cardiac output. The “wedge pressure” (LV preload) and cardiac output calculations are used to guide treatment.
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• Positive pressure ventilation: spontaneous breathing occurs because during inspiration, we create negative pressure inside the lungs and air rushes in to fill this low pressure. On a ventilator, inspiration occurs when the ventilator generates a positive pressure outside the patient which blows into the lungs. Thus, it is called positive pressure ventilation (PPV). PPV can delivered with intubation (insertion of a breathing tube). PPV benefits patients with decompensated CHF in the following ways:
o increased pressure inside the thorax will inhibit venous blood flow into the
o increased pressure inside the alveolus promotes the movement of fluid out
of the alveolus into the lung interstitium, thus improving ventilation to previously fluid filled alveoli.
o ventilated patients require little of no work to breathe. Therefore,
ventilation allows the patient to rest, which is a significant factor in patients who have very high respiratory rates and become exhausted just from the work to breathe.
• Intra-aortic balloon pump (IABP): a long skinny “balloon” is inserted into the
femoral artery and threaded up into the thoracic and abdominal aorta. During systole, the balloon very rapidly deflates. During diastole, the balloon very rapidly inflates. The computer that controls the balloon is connected to the patient’s ECG so that timing will be accurate. Because IABP is invasive and expensive, it is only used when drugs doses are maximized or drug use is limited because of hypotension. It is not a “first line” treatment. The IABP benefits patients with decompensated CHF in the following ways:
o rapid deflation during systole results in a low pressure aorta. This results
in a much reduced afterload for the left ventricle, which promotes ventricular emptying. A ventricle that empties easily will become will be smaller during both systole and diastole. Because preload is end-diastolic volume (EDV), using the IABP will decrease preload. Since both afterload and preload are reduced, ventricular wall stress will also be decreased. Because cardiac work is related to ventricular wall stress, cardiac work is decreased.
o inflation during diastole will increase diastolic aortic pressure and thus
perfusion pressure to the whole body during diastole. This includes the myocardium.
o coronary blood flow increases because of 2 factors: increasedaortic
diastolic pressure and decreased ventricular diastolic pressure.
• Left Ventricular Assist Devices (LVAD): this is a surgically implanted device
which is a battery powered pump that is connected to the aorta and left ventricle and simply pumps blood from the LV to the aorta, taking over a large portion of work that would have to be done by the LV. Many types are available and are still in evolution. Often used as a bridge before heart transplant only in very sick patients.
• Heart Transplant: for end stage heart disease. Limited by the availability of donor
hearts, but is a very good treatment with favorable 1, 5 and 10 year survival rates.
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Chronic Heart Failure Clinical scenario: a 70 year old male patient comes to see you in your family practice complaining of increasing fatigue and shortness of breath (SOB) during walking and other light activities over the past 2-3 months and swelling in the ankles. This patient has a cardiac history including 2 MI’s in the past and an echocardiagram showed an ejection fraction of 35%. The patient is non-compliant with medications and on occasion, will take a “water pill” to reduce the swelling in his legs, but takes no other medications. His vitals are: HR 80, BP 150/90, RR 16, SpO2 95%. His physical exam shows a JVP at 5 cm
when seated at 45 degrees upright, fine crackles in the lower 1/3 of both his lungs, ankle edema and an S3 is heard. Patients with chronic heart failure have some problems in common with acute heart failure (compare the 2 lists):
• decreased cardiac output • increased ventricular wall stress
o increased preload o increased afterload (usually, but not always)
o mild dyspnea, or dyspnea only on exertion o alveolar edema may or may not be present
• usually no distress or hypoxia • risk of dysrhythmias • risk of intracardiac thrombus (blood clot inside ventricle or atrium)
General Principles:
• the heart is not functioning as a good pump, but is performing better than the
patient who has developed acute heart failure. Cardiac output is low, filling pressures are high, afterload is high, and compensatory mechanisms (sympathetic nervous system and hormonal) are engaged for the long term. The primary goals will be to: reduce interstitial pulmonary edema, reduce preload, reduce afterload, increase cardiac output, and finally (and very importantly) to block the compensatory mechanisms to prevent their contribution to remodeling and apoptosis.
• If a patient is identified as high risk for dysrhythmias (such as ventricular
tachycardia or ventricular fibrillation) then they will need dysrhythmia prevention/treatment.
• Anti-coagulation is indicated for some patients with very poorly contracting
ventricles or atrial fibrillation (non-contracting atria). Anti-coagulation is required when stasis develops in the atrium or ventricle and the blood is at risk for producing a clot inside the cardiac chamber.
Conservative treatments:
• diet: a high salt and high water intake will increase preload. Restrictions are
placed on patients regarding 24 hour intake of NaCl and water. Other dietary recommendations (low cholesterol etc.) are important but will not be listed here.
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• exercise: an activity regime which is within the patient’s abilities is encouraged.
This might involve walking slowly for a period of time on a daily basis, or might can be more aggressive based on the patient’s functional abilities. Physical activity will help improve cardiac output as the heart becomes less deconditioned with intermittent stimulation of exercise.
• risk factor reduction: smoking, diabetes, hypertension and high cholesterol should
all be treated to prevent coronary artery disease.
Pharmacological Treatments: The 4 main drugs include:
1. ACE inhibitors: ACE inhibitors block the production of angiotensin II which is a
potent vasoconstrictor. Therefore, ACE inhibitors are vasodilators, which serves to reduce afterload. Decreasing afterload will increase cardiac output. Further, ACE inhibitors have been shown to decrease morbidity (sickness) and mortality in patients with chronic CHF. Note that ACE inhibitors are not used in acute CHF because of the hypotension that they can cause.
2. Beta blockers: beta blockers will reduce heart rate, myocardial work, and
contractility. All these factors will lower cardiac output. Therefore, beta blockers are contraindicated in acute CHF. However, evidence has shown that when used in the patient with chronic CHF, the patients have more symptoms (fatigue) in the first 3 months but then beyond that time, show benefit. Beta blockers must be started in very low doses (1/10 the target dose) and titrated upward slowly. Some patients will not tolerate beta blockade. Beta blockers have been shown to reduce morbidity and mortality. Patients in Stage D CHF often require adrenergic stimulation for survival and so cannot tolerate beta blockade. These patients would be, in fact, similar to acute CHF patients in this respect. Also recognize that beta blockers are a class II anti-arrhythmic and these properties might contribute to the reduced mortality seen in chronic CHF.
3. Diuretic: same mechanism as in acute CHF. Aim for a euvolemic state (not over
4. Digoxin: is not used in early chronic CHF, but is usually introduced as a 3rd or 4th
drug. It’s use has changed over the years with respect to which patients will benefit from receiving digoxin. It increases contractility through an increase in intracellular Ca concentrations. In patients with atrial fibrillation (common co-mobidity in CHF because the left atrium gets stretched and enlarged, resulting in abnormal electrical properties), digoxin plays a double role in reducing the ventricular rate by depressing the AV node.
Other drugs include (evidence is less convincing or still ongoing):
• nitroglycerine: same mechanism as in acute CHF. Used as a patch to give 12 hour
• angiotensin receptor blockers (ARB): these drugs block angiotensin II and
therefore lower afterload. Same principle at work as with ACE inhibitors.
• aldosterone antagonists (spironolactone): these drugs block the action of
aldosterone, one step in the biochemical pathway downstream from angiotensin
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II. Aldosterone is a vasoconstrictor and also reduces urine production. Therefore, spironolactone decreases preload and afterload.
• endothelin receptor antagonists: endothelins are vasoconstrictors. New drug under
 Note #1: positive inotropy through beta stimulation is a logical approach to use in
chronic heart failure. Past evidence, however, has shown that there is no benefit to using beta agonists and recent evidence shows that chronic beta stimulation is cardiotoxic. Digoxin is the only positive inotrope currently used in chronic CHF.
 Note #2: calcium channel blockers are not part of the chronic CHF
pharmacological regimen, even though they can reduce afterload.
Invasive treatments: Although pharmacologic treatment represents the vast majority of CHF treatment, there are some novel approaches, most experimental, that are being tested to treat CHF. These items will not be examined. For more information on this section, please see the reference below.
• LVAD’s, heart transplant, artificial heart: as listed under acute CHF • cardiac resynchronization (biventricular pacing): in order for the heart to beat at
maximum efficiency, it must be depolarized using normal conducting pathways, with physiological timing. Failure to do so will result in sub-optimal timing between the atria and ventricles, as well as sub-optimal mechanics of LV and RV contraction. Artificial pacing of both ventricles and the atria is an attempt to improve the timing and mechanics of a failing heart that has an abnormal conduction system. Newer treatment with good results.
• dynamic cardiomyoplasty: a sheet of latissumus dorsi skeletal muscle is wrapped
around the heart and the skeletal muscle is paced, to contract with cardiac contractions. Is experimental and not a mainstream treatment.
• ventriculectomy: the suffix “-ectomy” means “removal of”. Ventriculectomy is
the removal of part of the ventricle to reduce its size. By decreasing both radius and non-contracile scars or aneurysms of the ventricle, the wall tension is reduced and contractility is increased. Is experimental and not a mainstream treatment.
• myocardial restraint devices: non-contracting, inelastic splints are surgically
placed around the heart to prevent further dilation. Is experimental and not a mainstream treatment.
• cellular transplant: cardiac myocytes do not regenerate, but skeletal myocytes do.
Skeletal myoblasts are transplanted autologously (patient’s own cells) into the heart with the hopes that viable skeletal myoblasts can replace infarcted myocardium. Is experimental and not a mainstream treatment.
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www.medigraphic.org.mx CONFERENCIAS MAGISTRALES Opioids for the treatment of non-cancer pain * Professor of Anesthesiology and Medicine. Vice-Chair for Clinical Affairs. Department of Anesthesiology,University at Buffalo. Chief, Pain Medicine and Professor of Oncology. Roswell Park Cancer Institute. INTRODUCTION gested by the WHO step ladder, portending that it may not be appropriate